Search results for: Umberto M. Marinari

Items from 1 to 20 out of 24 results

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HO‐1 downregulation favors BRAF^V600 melanoma cell death induced by Vemurafenib/PLX4032 and increases NK recognition

Anna L. Furfaro, Selene Ottonello, Giulia Loi, Irene Cossu, more

International Journal of Cancer > 146 > 7 > 1950 - 1962

Heme oxygenase 1 (HO‐1) plays a pivotal role in preventing cell damage. Indeed, through the antioxidant, antiapoptotic and anti‐inflammatory properties of its metabolic products, it favors cell adaptation against different stressors. However, HO‐1 induction has also been related to the gain of resistance to therapy in different types of cancers and its involvement in cancer immune‐escape has been...

article

HO-1 down-regulation increases the efficacy of BRAFV600E inhibition-based therapy in primary melanoma cells

Anna Lisa Furfaro, Gabriella Pietra, Irene Cossu, Umberto M. Marinari, more

Free Radical Biology and Medicine > 2017 > 108 > S1 > S64

Heme oxygenase 1 (HO-1) plays a key role in maintaining cell redox balance. Under stress conditions, HO-1 is up-regulated and generates bilirubin, ferritin and carbon monoxide, with antioxidant, antiapoptotic and anti-inflammatory properties [Jozkowicz et al., 2007]. HO-1 induction favors cancer progression [Furfaro et al., 2016] and its involvement in tumor resistance to therapy [Was et al., 2006]...

article

Differentiation modifies Bach1 dependent regulation of HO-1 expression and increases sensitivity to oxidative stress in neuroblastoma cells

Sabrina Piras, Lorenzo Brondolo, Anna Lisa Furfaro, Mario Passalacqua, more

Free Radical Biology and Medicine > 2017 > 108 > S1 > S80

Neuronal adaptation to oxidative stress is crucial to prevent degenerative diseases. The role of the Nrf2/HO-1 system in cell response to hydrogen peroxide (H₂O₂) has been investigated using SH-SY5Y neuroblastoma cells as undifferentiated or after differentiation with all-trans retinoic acid (ATRA). We showed that undifferentiated cells resisted to oxidative stimulus and up-regulated HO-1 which was...

article

ATRA-induced neuronal differentiation reduces cell ability to adapt to oxidative stress: role of Nrf2 and HO-1

Sabrina Piras, Anna Lisa Furfaro, Cinzia Domenicotti, Nicola Traverso, more

Free Radical Biology and Medicine > 2016 > 96 > S1 > S49

article

Monomeric Aβ1–42 and RAGE: key players in neuronal differentiation

Sabrina Piras, Anna L. Furfaro, Alessandra Piccini, Mario Passalacqua, more

Neurobiology of Aging > 2014 > 35 > 6 > 1301-1308

The aggregation of amyloid-β (Aβ) peptides plays a crucial role in the onset and progression of Alzheimer's disease. Monomeric form of Aβ, indeed, could exert a physiological role. Considering the anti-oligomerization property of all-trans retinoic acid (ATRA), the involvement of monomeric Aβ1–42 in ATRA-induced neuronal differentiation has been investigated. Four-day ATRA treatment increases β-secretase...

article

Processing of the amyloid precursor protein: Role of protein kinase C and myosin IIB

Francesca Argellati, Cinzia Domenicotti, Maria A. Pronzato, Umberto M. Marinari, more

Alzheimer's & Dementia > 2009 > 5 > 4(S) > P493

article

Mechanisms of BSO (L-buthionine-S,R-sulfoximine)-induced cytotoxic effects in neuroblastoma

Barbara Marengo, Chiara De Ciucis, Daniela Verzola, Vito Pistoia, more

Free Radical Biology and Medicine > 2008 > 44 > 3 > 474-482

Glutathione (GSH) depletion is widely used to sensitize cells to anticancer treatment inducing the progression of programmed cell death and overcoming chemoresistance. It has been reported that neuroblastoma cells with MYCN amplification are unable to start TRAIL-dependent death and MYCN, in concert with cytotoxic drugs, efficiently induces the mitochondrial pathway of apoptosis through oxidative...

article

PKC signaling in oxidative hepatic damage

Mariapaola Nitti, Maria A. Pronzato, Umberto M. Marinari, Cinzia Domenicotti

Molecular Aspects of Medicine > 2008 > 29 > 1-2 > 36-42

Protein kinase C (PKC) is a family of isoenzymes differently involved in cell response to injury and many studies describe their role as “stress sensors”. Oxidative stress is strictly involved in the pathogenesis of chronic liver diseases including alcohol- or drug-induced hepatotoxicity, iron overload, hepatitis and hepatocarcinoma development, but molecular mechanisms are not really defined. A crucial...

article

Downregulation of myosin II-B by siRNA alters the subcellular localization of the amyloid precursor protein and increases amyloid-β deposition in N2a cells

Sara Massone, Francesca Argellati, Mario Passalacqua, Andrea Armirotti, more

Biochemical and Biophysical Research Communications > 2007 > 362 > 3 > 633-638

The Alzheimer’s disease (AD) brain pathology is characterized by extracellular deposits of amyloid-β (Aβ) peptides and intraneuronal fibrillar structures. These pathological features may be functionally linked, but the mechanism by which Aβ accumulation relates to neuronal degeneration is still poorly understood. Aβ peptides are fragments cleaved from the amyloid precursor protein (APP), a transmembrane...

article

PKC delta and NADPH oxidase in AGE-induced neuronal death

Mariapaola Nitti, Anna L. Furfaro, Nicola Traverso, Patrizio Odetti, more

Neuroscience Letters > 2007 > 416 > 3 > 261-265

Advanced glycation end product (AGE) accumulation in brain is believed to contribute to neuronal death in several neurodegenerative diseases. Neurons exposed to AGEs undergo oxidative stress, but the molecular mechanisms able to induce ROS generation and cell death are not yet clear. In this work, we exposed SH-SY5Y neuroblastoma cells to glycated albumin, as a model of AGE-modified protein, and we...

article

Amyloid precursor protein processing: Role of peroxisome proliferator-activated receptor-gamma

Roberta Ricciarelli, Sara Massone, Cristina d’Abramo, Umberto M. Marinari, more

Alzheimer's & Dementia: The Journal of the Alzheimer's Association > 2006 > 2 > 3 Supplement > S539

article

Supplementation with N-acetylcysteine and taurine failed to restore glutathione content in liver of streptozotocin-induced diabetics rats but protected from oxidative stress

Stefania Patriarca, Anna Lisa Furfaro, Cinzia Domenicotti, Patrizio Odetti, more

BBA - Molecular Basis of Disease > 2005 > 1741 > 1-2 > 48-54

Rats were rendered diabetic with streptozotocin and supplemented or not with N-acetylcysteine (NAC) and taurine (TAU). The liver was examined for the quantity of glutathione (GSH), both total and oxidised (GSSG), by HPLC assay. Moreover, the liver expression of gamma-glutamyl-cysteine synthetase, cysteine dioxygenase and heme oxygenase 1 was evaluated. Streptozotocin-diabetic rats showed decreased...

article

Central role of PKCδ in glycoxidation-dependent apoptosis of human neurons

Mariapaola Nitti, Cristina d'Abramo, Nicola Traverso, Daniela Verzola, more

Free Radical Biology and Medicine > 2005 > 38 > 7 > 846-856

Accumulation of advanced glycation end products (AGEs) induces alterations in the intracellular redox balance, leading cells to functional injury. Current literature reports that intracellular signaling triggered by the interaction of AGEs with their specific receptors RAGEs depends on the cell type and the state of activation/stress. In this work, NT2 human neurons were exposed for 48 h to glycated...

article

CD36 overexpression in human brain correlates with β-amyloid deposition but not with Alzheimer's disease

Roberta Ricciarelli, Cristina d'Abramo, Jean-Marc Zingg, Luca Giliberto, more

Free Radical Biology and Medicine > 2004 > 36 > 8 > 1018-1024

Scavenger receptors recently have been related to Alzheimer's disease, although it is still unclear whether they contribute to the pathogenesis of the disease or reflect an inflammatory response to the deposition of amyloid β-protein (Aβ). In this study we demonstrate that CD36, a class B scavenger receptor, is highly expressed in the cerebral cortex of Alzheimer's disease patients and cognitively...

article

A novel role of protein kinase C-δ in cell signaling triggered by glutathione depletion

Cinzia Domenicotti, Barbara Marengo, Mariapaola Nitti, Daniela Verzola, more

Biochemical Pharmacology > 2003 > 66 > 8 > 1521-1526

Current evidence demonstrates that protein kinase C (PKC) belongs to a group of cell-signaling molecules that are sensitive targets for redox modifications and functional alterations that mediate oxidant-induced cellular responses. Our studies have demonstrated that diminished intracellular GSH was associated to inactivation of classic isoforms and increased activity of novel PKCs, and triggered molecular...

article

Diabetes impairs the enzymatic disposal of 4-hydroxynonenal in rat liver

Nicola Traverso, Stefano Menini, Patrizio Odetti, M. Adelaide Pronzato, more

Free Radical Biology and Medicine > 2002 > 32 > 4 > 350-359

This study assesses whether the HNE accumulation we formerly observed in liver microsomes and mitochondria of BB/Wor diabetic rats depends on an increased rate of lipoperoxidation or on impairment of enzymatic removal. There are three main HNE metabolizing enzymes: glutathione-S-transferase (GST), aldehyde dehydrogenase (ALDH), and alcohol dehydrogenase (ADH). In this study we show that GST and ALDH...

article

Glutathione depletion induces apoptosis of rat hepatocytes through activation of protein kinase C novel isoforms and dependent increase in AP-1 nuclear binding

Cinzia Domenicotti, Dimitri Paola, Antonella Vitali, Mariapaola Nitti, more

Free Radical Biology and Medicine > 2000 > 29 > 12 > 1280-1290

Treatment of isolated rat hepatocytes with the glutathione depleting agents L-buthionine-S,R-sulfoximine or diethylmaleate reproduced various cellular conditions of glutathione depletion, from moderate to severe, similar to those occurring in a wide spectrum of human liver diseases. To evaluate molecular changes and possible cellular dysfunction and damage consequent to a pathophysiologic level of...

article

Oxidative Stress Induces Increase in Intracellular Amyloid β-Protein Production and Selective Activation of βI and βII PKCs in NT2 Cells - Volume 268, Number 2 (2000), pages 642-646 (doi:10.1006/bbrc.2000.2164)

Dimitri Paola, Cinzia Domenicotti, Mariapaola Nitti, Antonella Vitali, more

Biochemical and Biophysical Research Communications > 2000 > 272 > 1 > 309

article

Oxidative Stress Induces Increase in Intracellular Amyloid β-Protein Production and Selective Activation of βI and βII PKCs in NT2 Cells

Dimitri Paola, Cinzia Domenicotti, Mariapaola Nitti, Antonella Vitali, more

Biochemical and Biophysical Research Communications > 2000 > 268 > 2 > 642-646

Amyloid β-protein (Aβ) aggregation produces an oxidative stress in neuronal cells that, in turn, may induce an amyloidogenic shift of neuronal metabolism. To investigate this hypothesis, we analyzed intra- and extracellular Aβ content in NT2 differentiated cells incubated with 4-hydroxy-2,3-nonenal (HNE), a major product of lipid peroxidation. In parallel, we evaluated protein kinase C (PKC) isoenzymes...

article

Lipoperoxidation in hepatic subcellular compartments of diabetic rats - A consequence of cell injury?

Nicola Traverso, Stefano Menini, Patrizio Odetti, M. Adelaide Pronzato, more

Free Radical Biology and Medicine > 1999 > 26 > 5-6 > 538-547

It is known that an accumulation of lipoperoxidative aldehydes malondialdehyde (MDA) and 4-hydroxynonenal (HNE) takes place in liver mitochondria during aging. The existence and role of an increased extra- and intra-cellular oxidative stress in diabetes, an aging-accelerating disease, is currently under discussion. This report offers evidence that lipoperoxidative aldehydes accumulate in liver microsomes...

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Search results for: Umberto M. Marinari

HO‐1 downregulation favors BRAF^V600 melanoma cell death induced by Vemurafenib/PLX4032 and increases NK recognition

HO-1 down-regulation increases the efficacy of BRAFV600E inhibition-based therapy in primary melanoma cells

Differentiation modifies Bach1 dependent regulation of HO-1 expression and increases sensitivity to oxidative stress in neuroblastoma cells

ATRA-induced neuronal differentiation reduces cell ability to adapt to oxidative stress: role of Nrf2 and HO-1

Monomeric Aβ1–42 and RAGE: key players in neuronal differentiation

Processing of the amyloid precursor protein: Role of protein kinase C and myosin IIB

Mechanisms of BSO (L-buthionine-S,R-sulfoximine)-induced cytotoxic effects in neuroblastoma

PKC signaling in oxidative hepatic damage

Downregulation of myosin II-B by siRNA alters the subcellular localization of the amyloid precursor protein and increases amyloid-β deposition in N2a cells

PKC delta and NADPH oxidase in AGE-induced neuronal death

Amyloid precursor protein processing: Role of peroxisome proliferator-activated receptor-gamma

Supplementation with N-acetylcysteine and taurine failed to restore glutathione content in liver of streptozotocin-induced diabetics rats but protected from oxidative stress

Central role of PKCδ in glycoxidation-dependent apoptosis of human neurons

CD36 overexpression in human brain correlates with β-amyloid deposition but not with Alzheimer's disease

A novel role of protein kinase C-δ in cell signaling triggered by glutathione depletion

Diabetes impairs the enzymatic disposal of 4-hydroxynonenal in rat liver

Glutathione depletion induces apoptosis of rat hepatocytes through activation of protein kinase C novel isoforms and dependent increase in AP-1 nuclear binding

Oxidative Stress Induces Increase in Intracellular Amyloid β-Protein Production and Selective Activation of βI and βII PKCs in NT2 Cells - Volume 268, Number 2 (2000), pages 642-646 (doi:10.1006/bbrc.2000.2164)

Oxidative Stress Induces Increase in Intracellular Amyloid β-Protein Production and Selective Activation of βI and βII PKCs in NT2 Cells

Lipoperoxidation in hepatic subcellular compartments of diabetic rats - A consequence of cell injury?

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